PA23.3-4 | Peptic Ulcer Disease & Gastric Carcinoma — Summary & Reflection

REFLECT

Take a few minutes to consolidate your learning with these questions:

1. A 60-year-old woman has pernicious anaemia and autoimmune gastritis. Her endoscopy shows a 2.5 cm ulcer in the gastric body. List THREE features you would look for on endoscopy and biopsy to distinguish a benign from a malignant ulcer.

1. Draw (or mentally sketch) the aggressive-vs-defensive factor balance for PUD. For each of the following drugs, predict which side of the balance they affect and how: (a) omeprazole, (b) misoprostol, (c) amoxicillin (triple therapy), (d) aspirin.

1. A patient with linitis plastica has a positive Virchow node and Krukenberg tumours. Explain each finding using the routes of spread you have learned.

1. Why does H. pylori cause duodenal ulcer in some patients and gastric carcinoma in others? Think about antrum-predominant vs pangastritis and what each pattern does to acid secretion.

KEY TAKEAWAYS

Key take-aways from this module:

• Gastritis sets the stage: Type B (H. pylori, antrum) → PUD; pangastritis/atrophy → cancer risk. Type A (autoimmune, corpus) → pernicious anaemia + cancer risk.

• PUD pathogenesis = imbalance of aggressive factors (H. pylori, NSAIDs, acid/pepsin, smoking) over defensive factors (mucus-bicarbonate, prostaglandins, mucosal blood flow). H. pylori attacks both sides.

• Benign ulcer — punched-out, clean base, radiating folds, < 2 cm. Malignant ulcer — heaped irregular margins, necrotic base, interrupted folds. Biopsy ALL gastric ulcers.

• Four zones of chronic peptic ulcer histology (lumen → depth): Necrotic → Inflammatory → Granulation → Scar (NIGS).

• Complications of PUD: Haemorrhage (most common), Perforation (anterior DU), Penetration (posterior DU → pancreas), Obstruction (pyloric fibrosis), Malignancy (gastric only, rare).

• Gastric carcinoma pathogenesis: H. pylori → chronic gastritis → intestinal metaplasia → dysplasia → carcinoma (Correa's cascade; intestinal type). Diffuse type: E-cadherin loss, signet-ring cells, linitis plastica — NOT from metaplasia.

• Lauren classification: Intestinal type (gland-forming, H. pylori-related, better prognosis) vs Diffuse type (signet-ring, no glands, E-cadherin loss, worse prognosis).

• Spread: Virchow node (left supraclavicular, Troisier sign), Krukenberg tumour (bilateral ovaries, transcoelomic), Sister Mary Joseph nodule (umbilicus). Late presentation → poor prognosis worldwide.